The spontaneously hypertensive rat (SHR) provides the best available animal model of human essential hypertension. There is considerable evidence that brain mechanisms play an important role in the onset of hypertensive disease in these animals and that a crucial phase in its development occurs at the age of 6-8 weeks. The prominent theory in the field suggests that a hyperreactivity to environmental stimuli, mediated by a group of brain structures forming a system producing the defense reaction, is the cause of early episodes of elevated pressure. These trigger long term changes that sustain the adult hypertension. Any increase in blood pressure would be expected to be opposed by control systems "buffering" increases in pressure by decreasing sympathetic activity and heart rate. These control systems are termed the baroreceptor reflexes. In the present work we consider two alternative hypotheses to explain the hyperresponsiveness: 1. the defense reaction system is internally hyperactive and/or hypersensitive; or 2. the baroreceptor reflex system is relatively ineffective due to an inherent dysfunction in the reflex pathways or an enhanced ability of the defense reaction system to suppress reflex function. To test the viability of the second hypothesis, we propose to directly measure the effectiveness of the baroreceptor reflexes in young (6-8 week) SHR and two strains of normotensive rat. The effectiveness is expressed as reflex gain which is defined as the ratio of the change in sympathetic activity or heart rate to the change in blood pressure. We propose to make these measurements in an awake animal, free of anesthetics. If reduced reflexes are involved in the onset of SHR hypertension, it would suggest the more attention should be given the baroreceptor reflex function in an effort to improve therapeutic and diagnostic techniques in human hypertension.